a transcriptional co-regulatory protein. Proposed to mediate activation of the JNK pathway and apoptosis via ASK1 in response to signaling from FAS and TGF-betaR2. Glucose deprivation activates the ASK1-SEK1-JNK1-HIPK1 pathway, relocalizing Daxx from the nucleus to the cytoplasm, where Daxx binds to ASK1, and subsequently leads to ASK1 oligomerization. Interaction with HSP27 may prevent interaction with TGF-betaR2 and ASK1 and block DAXX-mediated apoptosis. Seems to act as a transcriptional co- repressor and inhibits PAX3 and ETS1 through direct protein- protein interaction. Its transcription repressor activity is modulated by recruiting it to subnuclear compartments like the nucleolus or PML/POD/ND10 nuclear bodies through interactions with MCSR1 and PML, respectively. Two alternatively spliced isoforms have been described. Note: This description may include information from UniProtKB.
Protein type: Apoptosis; Transcription, coactivator/corepressor; Nucleolus; Nuclear receptor co-regulator
Molecular Function: protein binding; enzyme binding; protein homodimerization activity; androgen receptor binding; histone binding; p53 binding; ubiquitin protein ligase binding; heat shock protein binding; receptor signaling protein activity; protein N-terminus binding; protein kinase activator activity; protein kinase binding; transcription factor binding; transcription corepressor activity
Biological Process: chromatin remodeling; nucleosome assembly; cytokinesis after mitosis; regulation of transcription, DNA-dependent; transcription, DNA-dependent; viral reproduction; induction of apoptosis via death domain receptors; apoptosis; regulation of protein ubiquitination; positive regulation of protein kinase activity; androgen receptor signaling pathway; positive regulation of protein amino acid phosphorylation; negative regulation of transcription, DNA-dependent; activation of JNK activity
LTP: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.